Mitochondrial aconitase knockdown attenuates paraquat-induced dopaminergic cell death via decreased cellular metabolism and release of iron and H₂O₂. - sprookjes - yvandenbroek - TriplyDB

Mitochondrial aconitase knockdown attenuates paraquat-induced dopaminergic cell death via decreased cellular metabolism and release of iron and H₂O₂.

Mitochondrial aconitase knockdown attenuates paraquat-induced dopaminergic cell death via decreased cellular metabolism and release of iron and H₂O₂.

http://www.wikidata.org/entity/Q35240549

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Mitochondrial involvement and oxidative stress in temporal lobe epilepsy Oxidative stress and pulmonary fibrosis Metabolic Investigations of the Molecular Mechanisms Associated with Parkinson's Disease Nicotinamide nucleotide transhydrogenase (Nnt) links the substrate requirement in brain mitochondria for hydrogen peroxide removal to the thioredoxin/peroxiredoxin (Trx/Prx) system.Alterations in energy/redox metabolism induced by mitochondrial and environmental toxins: a specific role for glucose-6-phosphate-dehydrogenase and the pentose phosphate pathway in paraquat toxicity Thioredoxin reductase deficiency potentiates oxidative stress, mitochondrial dysfunction and cell death in dopaminergic cells Glyphosate, pathways to modern diseases III: Manganese, neurological diseases, and associated pathologies.Generation of reactive oxygen species in 1-methyl-4-phenylpyridinium (MPP+) treated dopaminergic neurons occurs as an NADPH oxidase-dependent two-wave cascade.High-Resolution Respirometry for Simultaneous Measurement of Oxygen and Hydrogen Peroxide Fluxes in Permeabilized Cells, Tissue Homogenate and Isolated Mitochondria.Re-Cloning the N27 Dopamine Cell Line to Improve a Cell Culture Model of Parkinson's Disease.Prochelator BHAPI protects cells against paraquat-induced damage by ROS-triggered iron chelation Consequences of oxidative stress in age-related macular degeneration.Post-translational Activation of Glutamate Cysteine Ligase with Dimercaprol: A NOVEL MECHANISM OF INHIBITING NEUROINFLAMMATION IN VITRO.Targeting Oxidative Stress in Central Nervous System Disorders Exposure of aconitase to smoking-related oxidants results in iron loss and increased iron response protein-1 activity: potential mechanisms for iron accumulation in human arterial cells.The antidote effect of quinone oxidoreductase 2 inhibitor against paraquat-induced toxicity in vitro and in vivo.Mitochondrial susceptibility in a model of paraquat neurotoxicity.Metabolic control analysis of mitochondrial aconitase: influence over respiration and mitochondrial superoxide and hydrogen peroxide production.Glucose Metabolism and AMPK Signaling Regulate Dopaminergic Cell Death Induced by Gene (α-Synuclein)-Environment (Paraquat) Interactions.

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Mitochondrial aconitase knockdown attenuates paraquat-induced dopaminergic cell death via decreased cellular metabolism and release of iron and H₂O₂.

http://www.wikidata.org/entity/Q35240549

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2011 nî lūn-bûn

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011 թվականի մայիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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Mitochondrial aconitase knockd ...... and release of iron and H₂O₂.

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Mitochondrial aconitase knockd ...... and release of iron and H₂O₂.

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Mitochondrial aconitase knockd ...... and release of iron and H₂O₂.

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Mitochondrial aconitase knockd ...... and release of iron and H₂O₂.

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Mitochondrial aconitase knockd ...... and release of iron and H₂O₂.

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David Cantu

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Derek A Drechsel

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Manisha Patel

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Mitochondrial oxidative stress and increased seizure susceptibility in Sod2(-/+) mice

How mitochondria produce reactive oxygen species

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DJ-1 gene deletion reveals that DJ-1 is an atypical peroxiredoxin-like peroxidase

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Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen

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